Elevation of the blood lactate concentration by alkali therapy without requiring additional lactic acid accumulation: theoretical considerations.
A patient presented with lactic acidosis and severe acidemia; sodium bicarbonate was administered to titrate the very large hydrogen ion load. Coincident with this therapy, the blood lactate concentration rose from 21 to 27 mmole/L. In order to evaluate whether this rise in lactate could have occurred without requiring additional net lactic acid production, the effect of the hydrogen ion concentration on lactate distribution was evaluated. Data obtained from animal studies support the established hypothesis that lactate is distributed like other weak organic acids at steady-state; hence, alkalemia should favor a shift of lactate from the intracellular fluid (ICF) to the extracellular fluid (ECF). The authors calculated that the blood lactate concentration could rise by 50% without requiring net lactic acid accumulation when the severe acidemia was corrected by alkali therapy. Thus, an increase in lactate concentration of the magnitude observed during alkali therapy need not indicate a worsening of the metabolic picture in lactic acidosis.
D000468:Alkalies / Q000627:therapeutic use*; D001639:Bicarbonates / Q000627:therapeutic use; D016883:Diabetic Ketoacidosis / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007773:Lactates / Q000097:blood*; D008875:Middle Aged; D010629:Phenformin / Q000009:adverse effects
D000468:Alkalies; D001639:Bicarbonates; D007773:Lactates; D010629:Phenformin